Investigations will continue in two areas - 1) identification of subpopulations of IgG antibodies to DNA in murine SLE with studies of relative pathogenesis, and 2) identification of abnormal cell population(s) responsible for reduced autologous mixed lymphocyte reactions (auto MLR) in patients with active SLE with determination of etiol gy of the defect(s). Goals for the current year are to produce m noclonal murine subpopulations of anti-DNA antibodies using hybridomas and to study each antibody for pathogenesis by administering it (probably complexed with DNA) to healthy mice and by suppressing its production in murine lupus with anti-antibody. In auto-MLR studies, goals are to define the abnormal subpopulation of mononuclear cells (MNC) accounting for reduced reactivity in SLE and explore the possiblity of anti-lymphocyte antibodies (ALA) or immune complexes (IC) inducing the defect.